Polyurethane reinforced with micro/nano waste slag as a shielding panel for photons (experimental and theoretical study).

This study not only provides an innovative technique for producing rigid polyurethane foam (RPUF) composites, but it also offers a way to reuse metallurgical solid waste. Rigid polyurethane (RPUF) composite samples have been prepared with different proportions of iron slag as additives, with a range of 0-25% mass by weight. The process of grinding iron slag microparticles into iron slag nanoparticles powder was accomplished with the use of a high-energy ball mill. The synthesized samples have been characterized using Fourier Transform Infrared Spectroscopy, and Scanning Electron Microscope. Then, their radiation shielding properties were measured by using A hyper-pure germanium detector using point sources 241Am, 133 BA, 152 EU, 137Cs, and 60Co, with an energy range of 0.059-1.408 MeV. Then using Fluka simulation code to validate the results in the energy range of photon energies of 0.0001-100 MeV. The linear attenuation coefficient, mass attenuation coefficient, mean free path, half-value layer and tenth-value layer, were calculated to determine the radiation shielding characteristics of the composite samples. The calculated values are in good agreement with the calculated values. The results of this study showed that the gamma-ray and neutron attenuation parameters of the studied polyurethane composite samples have improved. Moreover, the effect of iron slag not only increases the gamma-ray attenuation shielding properties but also enhances compressive strength and the thermal stability. Which encourages us to use polyurethane iron-slag composite foam in sandwich panel manufacturing as walls to provide protection from radiation and also heat insulation.

Developing of Lead/Polyurethane Micro/Nano Composite for Nuclear Shielding Novel Supplies: γ-Spectroscopy and FLUKA Simulation Techniques.

In this work, the effect of adding Pb nano/microparticles in polyurethane foams to improve thermo-physical and mechanical properties were investigated. Moreover, an attempt has been made to modify the micron-sized lead metal powder into nanostructured Pb powder using a high-energy ball mill. Two types of fillers were used, the first is Pb in micro scale and the second is Pb in nano scale. A lead/polyurethane nanocomposite is made using the in-situ polymerization process. The different characterization techniques describe the state of the dispersion of fillers in foam. The effects of these additions in the foam were evaluated, Fourier transform infrared spectroscopy (FTIR), scanning electron microscopy (SEM), transmission electron microscopy (TEM), and X-ray diffraction (XRD) have all been used to analyze the morphology and dispersion of lead in polyurethane. The findings demonstrate that lead is uniformly distributed throughout the polyurethane matrix. The compression test demonstrates that the inclusion of lead weakens the compression strength of the nanocomposites in comparison to that of pure polyurethane. The TGA study shows that the enhanced thermal stability is a result of the inclusion of fillers, especially nanofillers. The shielding efficiency has been studied, MAC, LAC, HVL, MFP and Zeff were determined either experimentally or by Monte Carlo calculations. The nuclear radiation shielding properties were simulated by the FLUKA code for the photon energy range of 0.0001-100 MeV.

Picolinic Acid, a Catabolite of Tryptophan, Has an Anabolic Effect on Bone In Vivo.

Fractures attributable to osteoporosis have a severe impact on our older population. Reports of side effects with commonly prescribed osteoporosis drugs have led to the investigation of new and safer treatments with novel mechanisms of action. Picolinic acid (PIC), a catabolite of tryptophan, induces in vitro osteogenic differentiation of mesenchymal stem cells. Here we demonstrate that PIC has an anabolic effect on bone in vivo by increasing bone formation, bone mass, and bone strength in normal and ovariectomized C57BL/6 mice. Activation of the osteogenic pathways triggered this osteoanabolic response without any cross-related effects on mineral absorption or calciotropic hormones. Because PIC was also well tolerated and absorbed with no side effects, it is an ideal potential candidate for the treatment of osteoporosis. © 2020 American Society for Bone and Mineral Research.

Treatment with an inhibitor of fatty acid synthase attenuates bone loss in ovariectomized mice.

Bone and fat cells have an antagonistic relationship. Adipocytes exert a toxic effect on bone cells in vitro through the secretion of fatty acids, which are synthesized by fatty acid synthase (FAS). Inhibition of FAS in vitro rescues osteoblasts from fat-induced toxicity and cell death. In this study, we hypothesized that FAS inhibition would mitigate the loss of bone mass in ovariectomized (OVX) mice. We treated OVX C57BL/6 mice with cerulenin (a known inhibitor of FAS) for 6 weeks and compared their bone phenotype with vehicle-treated controls. Cerulenin-treated mice exhibited a significant decrease in body weight, triglycerides, leptin, and marrow and subcutaneous fat without changes in serum glucose or calciotropic hormones. These effects were associated with attenuation of bone loss and normalization of the bone phenotype in the cerulenin-treated OVX group compared to the vehicle-treated OVX group. Our results demonstrate that inhibition of FAS enhances bone formation, induces uncoupling between osteoblasts and osteoclasts, and favors mineralization, thus providing evidence that inhibition of FAS could constitute a new anabolic therapy for osteoporosis.

Characterizing the molecular phenotype of an Atp7a(T985I) conditional knock in mouse model for X-linked distal hereditary motor neuropathy (dHMNX).

ATP7A is a P-type ATPase essential for cellular copper (Cu) transport and homeostasis. Loss-of-function ATP7A mutations causing systemic Cu deficiency are associated with severe Menkes disease or its milder allelic variant, occipital horn syndrome. We previously identified two rare ATP7A missense mutations (P1386S and T994I) leading to a non-fatal form of motor neuron disorder, X-linked distal hereditary motor neuropathy (dHMNX), without overt signs of systemic Cu deficiency. Recent investigations using a tissue specific Atp7a knock out model have demonstrated that Cu plays an essential role in motor neuron maintenance and function, however the underlying pathogenic mechanisms of ATP7A mutations causing axonal degeneration remain unknown. We have generated an Atp7a conditional knock in mouse model of dHMNX expressing Atp7a(T985I), the orthologue of the human ATP7A(T994I) identified in dHMNX patients. Although a degenerative motor phenotype is not observed, the knock in Atp7a(T985I/Y) mice show altered Cu levels within the peripheral and central nervous systems, an increased diameter of the muscle fibres and altered myogenin and myostatin gene expression. Atp7a(T985I/Y) mice have reduced Atp7a protein levels and recapitulate the defective trafficking and altered post-translational regulatory mechanisms observed in the human ATP7A(T994I) patient fibroblasts. Our model provides a unique opportunity to characterise the molecular phenotype of dHMNX and the time course of cellular events leading to the process of axonal degeneration in this disease.

The ratio of macronutrients, not caloric intake, dictates cardiometabolic health, aging, and longevity in ad libitum-fed mice.

The fundamental questions of what represents a macronutritionally balanced diet and how this maintains health and longevity remain unanswered. Here, the Geometric Framework, a state-space nutritional modeling method, was used to measure interactive effects of dietary energy, protein, fat, and carbohydrate on food intake, cardiometabolic phenotype, and longevity in mice fed one of 25 diets ad libitum. Food intake was regulated primarily by protein and carbohydrate content. Longevity and health were optimized when protein was replaced with carbohydrate to limit compensatory feeding for protein and suppress protein intake. These consequences are associated with hepatic mammalian target of rapamycin (mTOR) activation and mitochondrial function and, in turn, related to circulating branched-chain amino acids and glucose. Calorie restriction achieved by high-protein diets or dietary dilution had no beneficial effects on lifespan. The results suggest that longevity can be extended in ad libitum-fed animals by manipulating the ratio of macronutrients to inhibit mTOR activation.